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沙门氏菌感染期间B细胞中的促炎和抗炎反应。

Pro-inflammatory and anti-inflammatory responses in B cells during Salmonella infection.

作者信息

Perez-Lopez Araceli, Hernandez-Galicia Gabriela, Lopez-Bailon Luis Uriel, Gonzalez-Telona Ana D, Rosales-Reyes Roberto, Alpuche-Aranda Celia M, Santos-Preciado Jose I, Ortiz-Navarrete Vianney

机构信息

1Unidad de Medicina Experimental, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City, Mexico.

4Unidad de Investigación en Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México.Tlalnepantla, State of Mexico, Mexico.

出版信息

Eur J Microbiol Immunol (Bp). 2025 Mar 11;15(1):32-41. doi: 10.1556/1886.2024.00088. Print 2025 Mar 19.

DOI:10.1556/1886.2024.00088
PMID:40067375
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11925187/
Abstract

B-cells serve as a niche for Salmonella to establish a chronic infection, enabling bacteria to evade immune responses. One mechanism Salmonella uses to survive inside B-cells involves inhibiting the NLRC4 inflammasome activation, thereby preventing pyroptotic cell death. This study investigates whether Salmonella-infected B-cells can mount bactericidal responses to control intracellular bacteria. Our results show that Salmonella-infected B-cells can produce and release TNFα, IL-6, and IL-10, but not RANTES. Furthermore, priming B-cells with TNFα, IL-1β, or IFNγ enhances their bactericidal activity by promoting the production of reactive oxygen and nitrogen production species, reducing intracellular load. These results suggest that B-cells can clear Salmonella infection within a pro-inflammatory environment. However, the concurrent production of IL-10 may counteract the effects of pro-inflammatory cytokines, potentially modulating the immune response in the microenvironment.

摘要

B细胞为沙门氏菌建立慢性感染提供了一个生态位，使细菌能够逃避免疫反应。沙门氏菌在B细胞内存活所使用的一种机制涉及抑制NLRC4炎性小体的激活，从而防止细胞焦亡。本研究调查了感染沙门氏菌的B细胞是否能够产生杀菌反应以控制细胞内细菌。我们的结果表明，感染沙门氏菌的B细胞可以产生并释放TNFα、IL-6和IL-10，但不能产生RANTES。此外，用TNFα、IL-1β或IFNγ刺激B细胞可通过促进活性氧和氮产物的产生来增强其杀菌活性，从而减少细胞内负荷。这些结果表明，B细胞可以在促炎环境中清除沙门氏菌感染。然而，IL-10的同时产生可能会抵消促炎细胞因子的作用，从而可能调节微环境中的免疫反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f13/11925187/4dfe0114fe19/eujmi-15-032-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f13/11925187/0cd1db355337/eujmi-15-032-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f13/11925187/8fd9ca361c8f/eujmi-15-032-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f13/11925187/93c1d5210ccc/eujmi-15-032-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f13/11925187/4dfe0114fe19/eujmi-15-032-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f13/11925187/0cd1db355337/eujmi-15-032-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f13/11925187/8fd9ca361c8f/eujmi-15-032-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f13/11925187/93c1d5210ccc/eujmi-15-032-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f13/11925187/4dfe0114fe19/eujmi-15-032-g004.jpg

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Activation and pro-inflammatory cytokine production by unswitched memory B cells during SARS-CoV-2 infection.在 SARS-CoV-2 感染期间，未转换记忆 B 细胞的激活和促炎细胞因子产生。
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